Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5535
pubmed:dateCreated
2001-9-4
pubmed:abstractText
We show that high doses of salicylates reverse hyperglycemia, hyperinsulinemia, and dyslipidemia in obese rodents by sensitizing insulin signaling. Activation or overexpression of the IkappaB kinase beta (IKKbeta) attenuated insulin signaling in cultured cells, whereas IKKbeta inhibition reversed insulin resistance. Thus, IKKbeta, rather than the cyclooxygenases, appears to be the relevant molecular target. Heterozygous deletion (Ikkbeta+/-) protected against the development of insulin resistance during high-fat feeding and in obese Lep(ob/ob) mice. These findings implicate an inflammatory process in the pathogenesis of insulin resistance in obesity and type 2 diabetes mellitus and identify the IKKbeta pathway as a target for insulin sensitization.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents..., http://linkedlifedata.com/resource/pubmed/chemical/Aspirin, http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose, http://linkedlifedata.com/resource/pubmed/chemical/Chuk protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Dietary Fats, http://linkedlifedata.com/resource/pubmed/chemical/I-kappa B Kinase, http://linkedlifedata.com/resource/pubmed/chemical/Ikbkb protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Ikbke protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Insulin, http://linkedlifedata.com/resource/pubmed/chemical/Lipids, http://linkedlifedata.com/resource/pubmed/chemical/Prostaglandin-Endoperoxide Synthases, http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Insulin, http://linkedlifedata.com/resource/pubmed/chemical/Sodium Salicylate, http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0036-8075
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
293
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1673-7
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:11533494-Animals, pubmed-meshheading:11533494-Anti-Inflammatory Agents, Non-Steroidal, pubmed-meshheading:11533494-Aspirin, pubmed-meshheading:11533494-Blood Glucose, pubmed-meshheading:11533494-Cell Line, pubmed-meshheading:11533494-Dietary Fats, pubmed-meshheading:11533494-Gene Deletion, pubmed-meshheading:11533494-Gene Targeting, pubmed-meshheading:11533494-Glucose Tolerance Test, pubmed-meshheading:11533494-I-kappa B Kinase, pubmed-meshheading:11533494-Insulin, pubmed-meshheading:11533494-Insulin Resistance, pubmed-meshheading:11533494-Lipids, pubmed-meshheading:11533494-Liver, pubmed-meshheading:11533494-Male, pubmed-meshheading:11533494-Mice, pubmed-meshheading:11533494-Mice, Obese, pubmed-meshheading:11533494-Muscles, pubmed-meshheading:11533494-Obesity, pubmed-meshheading:11533494-Phosphorylation, pubmed-meshheading:11533494-Prostaglandin-Endoperoxide Synthases, pubmed-meshheading:11533494-Protein-Serine-Threonine Kinases, pubmed-meshheading:11533494-Rats, pubmed-meshheading:11533494-Rats, Zucker, pubmed-meshheading:11533494-Receptor, Insulin, pubmed-meshheading:11533494-Signal Transduction, pubmed-meshheading:11533494-Sodium Salicylate, pubmed-meshheading:11533494-Tumor Necrosis Factor-alpha
pubmed:year
2001
pubmed:articleTitle
Reversal of obesity- and diet-induced insulin resistance with salicylates or targeted disruption of Ikkbeta.
pubmed:affiliation
Joslin Diabetes Center and Department of Medicine, Harvard Medical School, Boston, MA 02215, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't